The Neuroprotective Effects of Education

Few would doubt the benefits of education. People who graduate from high school tend to earn more, and generally have more choices and a better quality of life than those who do not, and for those who finish college, the benefits are even bigger.

A good education may have other advantages. Research published in the past few years suggests that it can strengthen the brain, making it more resistant to the ravages of old age, and perhaps mitigating the damage that occurs after traumatic brain injury. [See Big Data on Healthy Brain Aging]

Research into the link between education and dementia began in the mid-1980s. Some of the early studies produced conflicting results, but overall the evidence suggests that a higher level of educational attainment is associated with both a decreased risk of Alzheimer's disease and the more-common, slower age-related cognitive decline.

These studies further suggest that the relationship between educational attainment and risk of dementia is more consistent in developed countries compared with developing ones. They also point to racial differences in the beneficial effects of education: Despite well-established disparities in the health status of blacks and whites, education beyond high school is more strongly associated with better lifelong health outcomes in blacks than whites.

Perhaps ironically, highly educated people also experience a faster rate of cognitive decline following a diagnosis of Alzheimer's than those with lower educational attainment, and this is likely linked to a faster rate of neurodegeneration. This may mean that that they are better able to compensate for the damage that occurs at the earliest stages of the disease, so symptoms begin to manifest only once the brain damage has become severe. It also means that after diagnosis, they are likely to die sooner.

Level of education is often closely associated with socioeconomic status, and the relationship between the two confounded the results obtained in some of the earlier studies, but more recent findings show that they are indeed independent of one another, and that education is by far the more significant factor.

Level of education may also accurately predict
the extent to which one will recover following traumatic brain injury (TBI).
Researchers from Johns Hopkins Medical School in Baltimore tracked the progress
of nearly 800 patients, all of whom had been admitted for rehabilitation after
moderate to severe TBI, and had at least one year of follow-up examinations.

Many researchers explain findings such as these in terms of cognitive reserve, a concept that stems from the many observations that some people can continue to function normally despite brain pathology.

The term 'cognitive reserve' was first used in a 1988 study, in which researchers from the University of California, San Diego examined the brains of 137 nursing home residents, all of whom had undergone neuropsychological testing before they died. While 10 of them had remained cognitively healthy-and had outperformed healthy individuals on the tests-post-mortem examination revealed in their brains the pathological changes associated with Alzheimer's.

These women also had heavier brains and more neurons than both the demented and healthy residents included in the study, leading the researchers to hypothesize that these extra cells provided a 'reserve' that made them better at coping with the damage caused by the disease. The idea is that there is a threshold at which deficits become apparent, and those with more reserve need more damage to reach it.

In support of this idea, a large multi-center study led by researchers at the University of Cambridge found that longer years in education were associated with decreased risk of dementia and greater brain weight, but bore no relationship to neuropathological changes.

"The idea of cognitive reserve stems from the observation that some people can cope better than others with brain changes or brain pathology," says Yaakov Stern, a professor of clinical neuropsychology at Columbia University. "It suggests that some people can take better advantage of their available brain resources by using more efficient, higher capacity, or more flexible cognitive approaches."

"The concept of cognitive reserve can be useful when it is well defined, [but often] it is not," says Ian Deary, a professor of psychology at the University of Edinburgh. "I admire the rigorous work that people like Stern have done in examining the mechanisms… and explaining what the idea means."

"In our own research, we found that education was associated with IQ-type scores in older age but not with more fundamental information processing," he continues. "Therefore, education might provide a small lifetime boost in complex thinking, but maybe not in the basic mechanics that underlie it."

In studies such as these, level of education and IQ score both serve as a proxy for cognitive reserve, and the effects of education are always seen to be 'dose-dependant': The more highly educated a person is, the more reserve they have and, consequently, the less susceptible they are to the normal and pathological brain changes that occur with age. (Another recent study showed that even just a few years of formal education can delay the onset of dementia, presumably by contributing to cognitive reserve.)

Other factors can also build reserve. "The evidence suggests that life experiences such as education, challenges at work, and other activities can work together in an additive fashion to impart more cognitive reserve," says Stern, adding that staying active and socially engaged could help build up the reserve. "It may be that one could develop a recipe for building reserve via specific interventions, such as classes or video games, but the research on that still needs to be done."

Comments

Cognitive Reserve

Ian H Robertson

5/23/2014 10:21:53 AM

Thanks for a very nice post. The way in which cognitive reserve protects against disease and injury may be linked to the norepinephrine/noradrenaline system: NE/NA reduces inflammation and amyloid plaque toxicity, as well as rescuing dopaminergic and cholinergic neurones. I have set out this theory in Neurobiology of Aging and would welcome comments:
http://download.journals.elsevierhealth.com/pdfs/journals/0197-4580/PIIS0197458012003193.pdf